The Spectrum of MR Detectable Cortical Microinfarcts: A Classification Study with 7-Tesla Postmortem MRI and Histopathology

Veluw, Susanne J. van; Zwanenburg, Jaco J.M.; Rozemüller, Annemieke; Luijten, Peter R.; Spliet, Wim G.M.; Biessels, Geert Jan

doi:10.1038/jcbfm.2014.258

Cited by 57 publications

(79 citation statements)

References 30 publications

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“…Recent radiologic-pathologic studies have shown that microinfarcts of approximately 1 to 2 mm can be detected on 3-and 7-Tesla in vivo MRI scans ( Figure 1C). 67,68 However, microinfarcts can be as small as 100 microns, 54,63 thus a large proportion of these lesions remain invisible on brain imaging. 10 The rapid development of imaging techniques and optimization of T1-and T2*-weighted MRI sequences, both on 7 Tesla and on lower field strength MRI, makes it likely that we will be able to quantify smaller lesions in vivo in the near future.…”

Section: Microinfarctsmentioning

confidence: 99%

Ischemic brain injury in cerebral amyloid angiopathy

Reijmer

Veluw

Greenberg

2015

J Cereb Blood Flow Metab

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Cerebral amyloid angiopathy (CAA) is a common form of cerebral small vessel disease and an important risk factor for intracerebral hemorrhage and cognitive impairment. While the majority of research has focused on the hemorrhagic manifestation of CAA, its ischemic manifestations appear to have substantial clinical relevance as well. Findings from imaging and pathologic studies indicate that ischemic lesions are common in CAA, including white-matter hyperintensities, microinfarcts, and microstructural tissue abnormalities as detected with diffusion tensor imaging. Furthermore, imaging markers of ischemic disease show a robust association with cognition, independent of age, hemorrhagic lesions, and traditional vascular risk factors. Widespread ischemic tissue injury may affect cognition by disrupting white-matter connectivity, thereby hampering communication between brain regions. Challenges are to identify imaging markers that are able to capture widespread microvascular lesion burden in vivo and to further unravel the etiology of ischemic tissue injury by linking structural magnetic resonance imaging (MRI) abnormalities to their underlying pathophysiology and histopathology. A better understanding of the underlying mechanisms of ischemic brain injury in CAA will be a key step toward new interventions to improve long-term cognitive outcomes for patients with CAA.

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Section: Microinfarctsmentioning

confidence: 99%

Ischemic brain injury in cerebral amyloid angiopathy

Reijmer

Veluw

Greenberg

2015

J Cereb Blood Flow Metab

Self Cite

123

102

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“…These focal elongated lesions were hyperintense on 7T FLAIR (0.8 mm isotropic voxels), restricted to the cortex and seemed to extend from the cortical surface, hyperintense on T2 (0.7 mm isotropic voxels), and hypointense on T1 (1.0 mm isotropic voxels). It was confirmed that these lesions were cortical CMIs using an MR-guided histopathology approach in post-mortem human brain tissue 6,7 .…”

Section: Introductionmentioning

confidence: 65%

“…2. Assess cortical CMIs on the in vivo 7T MR images as detailed in the steps below, using the following 7T rating criteria for CMIs: cortical CMIs are hyperintense on FLAIR (with or without a hypointense center), hyperintense on T2, hypointense on T1, detectable on at least two views of the brain (e.g., sagittal and transversal), restricted to the cortex, distinct from perivascular spaces, with a greatest dimension ≤4 mm 6,7 . 3.…”

Section: Assessing Cortical Microinfarcts On In Vivo 7t Mrimentioning

confidence: 99%

Assessing Cortical Cerebral Microinfarcts on High Resolution MR Images

Veluw

Biessels

Luijten

et al. 2015

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Cerebral microinfarcts are frequent findings in the post-mortem human brain, and are related to cognitive decline and dementia. Due to their small sizes it is challenging to study them on clinical MRI scans. It was recently demonstrated that cortical microinfarcts can be depicted with MRI scanners using high magnetic field strengths (7T). Based on this experience, a proportion of these lesions is also visible on lower resolution 3T MRI. These findings were corroborated with ex vivo imaging of post-mortem human brain tissue, accompanied by histopathological verification of possible cortical microinfarcts.Here an ex vivo imaging protocol is presented, for the purpose of validating MR observed cerebral microvascular pathology with histological evaluation. Furthermore, guidelines are provided for the assessment of cortical microinfarcts on both in vivo 7T and 3T MR images. These guidelines provide researchers with a tool to rate cortical microinfarcts on in vivo images of larger patient samples, to further unravel their clinical relevance in cognitive decline and dementia, and establish these lesions as a novel biomarker of cerebral small vessel disease. Video LinkThe video component of this article can be found at

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“…A recent post-mortem study of confirmed dementia cases found WMH pathology was consistent with microinfarcts, except for in juxtacortical lesion, which were enlarged perivascular spaces (34). Other research suggests ischemic, rather than small vessel disease, has a prominent role in WMH pathophysiology (35).…”

Section: The Pathophysiology and Development Of Wmhsmentioning

confidence: 99%

Brain Structural Connectivity in Late-Life Major Depressive Disorder

Smagula

Aizenstein

2016

Biological Psychiatry: Cognitive Neuroscience and Neuroimaging

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Disrupted brain connectivity might explain both the pathogenesis and consequences of late-life major depressive disorder (LLD). However, it remains difficult to ascertain whether and how specific circuits are affected. We reviewed literature regarding brain connectivity in LLD, and we specifically focused on the role of structural pathology. LLD is associated with greater levels of cerebrovascular disease, and greater levels of cerebrovascular disease are associated with both depression development and treatment responsiveness. Cerebrovascular disease is most often measured as white matter hyperintensity (WMH) burden, and histopathology studies suggest WMH reflect myelin damage and fluid accumulation (among other underlying pathology). WMHs appear as confluent caps around the ventricles (periventricular), as well as isolated lesions in the deep white matter. The underlying tissue damage and implications for brain connectivity may differ by WMH location or severity. WMHs are associated with lower white matter microstructural integrity (measured with diffusion tensor imaging) and altered brain function (measured with functional MRI). LLD is also associated with lower white matter microstructural integrity and grey matter loss which may also alter the network properties and function of the brain. Damage to brain structure reflected by WMH, reduced white matter microstructural integrity, and atrophy may affect brain function, and are therefore likely pathophysiological mechanisms of LLD. Additional research is needed to fully characterize the developmental course and pathology underlying these imaging markers, and to understand how structural damage explains LLD's various clinical manifestations.

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The Spectrum of MR Detectable Cortical Microinfarcts: A Classification Study with 7-Tesla Postmortem MRI and Histopathology

Cited by 57 publications

References 30 publications

Ischemic brain injury in cerebral amyloid angiopathy

Ischemic brain injury in cerebral amyloid angiopathy

Assessing Cortical Cerebral Microinfarcts on High Resolution MR Images

Brain Structural Connectivity in Late-Life Major Depressive Disorder

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